INHALED NITRIC-OXIDE FOR THE ADULT RESPIRATORY-DISTRESS SYNDROME
INHALED NITRIC-OXIDE FOR THE ADULT RESPIRATORY-DISTRESS SYNDROME
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DOI：
10.1056/nejm199302113280605
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发表时间：
1993-02-11
影响因子：
158.5
通讯作者：
ZAPOL, WM
中科院分区：
文献类型：
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作者：
ROSSAINT, R;FALKE, KJ;ZAPOL, WM
背景成人呼吸窘迫综合征的特征是肺动脉高压和静脉血从右向左分流。我们研究了吸入一氧化氮气体是否会引起通气肺区域的选择性血管舒张，从而降低肺动脉高压并改善气体交换。连续10例严重成人呼吸窘迫综合征患者中有9例吸入两种浓度的一氧化氮，每次40分钟。在一氧化氮吸入过程中，通过多种惰性气体消除技术测量血流动力学变量、气体交换和通气-灌注分布;将结果与前列环素静脉输注过程中获得的结果进行比较。7例患者连续吸入浓度为百万分之5至20（ppm）的一氧化氮治疗3至53天。吸入浓度为18 ppm的一氧化氮使平均（+/-SE）肺动脉压从37+/-3 mmHg降至30+/-2 mmHg（P = 0.008），肺内分流率从36+/-5%降至31+/-5%（P = 0.028）。动脉氧分压与吸入氧分数的比值（PaO 2/FiO 2）是动脉氧合效率的指标，在一氧化氮给药期间从152+/-15 mm Hg增加到199+/-23 mm Hg（P = 0.008），尽管平均动脉压和心输出量没有变化。前列环素的输注降低了肺动脉压，但增加了肺内分流，降低了PaO 2/FiO 2和全身动脉压。持续吸入一氧化氮可持续降低肺动脉压并增加PaO 2/FiO 2，持续3至53天。严重成人呼吸窘迫综合征患者吸入一氧化氮可通过改善通气与灌注的匹配降低肺动脉压并增加动脉氧合，而不产生全身血管舒张。需要进行随机、盲法试验来确定吸入一氧化氮是否会改善预后。
Background. The adult respiratory distress syndrome is characterized by pulmonary hypertension and right-to-left shunting of venous blood. We investigated whether inhaling nitric oxide gas would cause selective vasodilation of ventilated lung regions, thereby reducing pulmonary hypertension and improving gas exchange.Methods. Nine of 10 consecutive patients with severe adult respiratory distress syndrome inhaled nitric oxide in two concentrations for 40 minutes each. Hemodynamic variables, gas exchange, and ventilation-perfusion distributions were measured by means of multiple inert-gas-elimination techniques during nitric oxide inhalation; the results were compared with those obtained during intravenous infusion of prostacyclin. Seven patients were treated with continuous inhalation of nitric oxide in a concentration of 5 to 20 parts per million (ppm) for 3 to 53 days.Results. Inhalation of nitric oxide in a concentration of 18 ppm reduced the mean (+/-SE) pulmonary-artery pressure from 37+/-3 mm Hg to 30+/-2 mm Hg (P = 0.008) and decreased intrapulmonary shunting from 36+/-5 percent to 31+/-5 percent (P = 0.028). The ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen (PaO2/FiO2), an index of the efficiency of arterial oxygenation, increased during nitric oxide administration from 152+/-15 mm Hg to 199+/-23 mm Hg (P = 0.008), although the mean arterial pressure and cardiac output were unchanged. Infusion of prostacyclin reduced pulmonary-artery pressure but increased intrapulmonary shunting and reduced the PaO2/FiO2 and systemic arterial pressure. Continuous nitric oxide inhalation consistently lowered the pulmonary-artery pressure and augmented the PaO2/FiO2 for 3 to 53 days.Conclusions. Inhalation of nitric oxide by patients with severe adult respiratory distress syndrome reduces the pulmonary-artery pressure and increases arterial oxygenation by improving the matching of ventilation with perfusion, without producing systemic vasodilation. Randomized, blinded trials will be required to determine whether inhaled nitric oxide will improve outcome.